tbuckley/cabot-search huggingface dataset:
Diseases Transmitted from Animals to Man.
Journal: JAMA (1930)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Council on Foods and Nutrition
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Endoscopy International Open – recently published
Journal: Endoscopy (2016)

See also: Lumen-apposing covered self-expanding metal stent for management of benign gastrointestinal stricturesEndosc Int Open 2016; 04(01): E96-E101DOI: 10.1055/s-0041-108195 See also: The loop-forming method as a useful technique to rotate the endoscopic insertion tube shaftEndosc Int Open 2016; 04(02): E170-E174DOI: 10.1055/s-0041-109082 See also: Evaluation of interventional endoscopy unit efficiency metrics at a tertiary academic medical centerEndosc Int Open 2016; 04(02): E143-E148DOI: 10.1055/s-0041-108082
Editorial Board and Contents
Authors: Moran Furman, Joanna Schaffhausen, Paige Shaklee, Fred Kop, Ria Otten, Patrick Scheffmann, Silvia Arber, Anders Björklund, J Paul Bolam, Sarah Bottjer, Rui Costa, Ann Marie, Craig Barry, J Dickson, Chris Doe, Craig Garner, Yukiko Goda, Kenneth Harris, Nancy Ip, Meyer Jackson, Maria Karayiorgou, Robert Malenka, Mark Mattson, Freda Miller, Richard Morris, Maiken Nedergaard, Eric Nestler, Anna Roe, Hitoshi Sakano, Wolf Singer, Greg Stuart, Marc Tessier-Lavigne, Chris Walsh
Journal: Trends in Neurosciences (2018)
Awards, Appointments, Announcements
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Awards, Appointments, Announcements Get access JNCI: Journal of the National Cancer Institute, Volume 83, Issue 6, 20 March 1991, Pages 398–399, https://doi.org/10.1093/jnci/83.6.398 Published: 20 March 1991
New and Nonofficial Remedies, 1922.
Journal: JAMA (1922)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Endoscopy International Open – recently published
Journal: Endoscopy (2016)

See also: Hill classification is superior to the axial length of a hiatal hernia for assessment of the mechanical anti-reflux barrier at the gastroesophageal junctionEndosc Int Open 2016; 04(03): E311-E317DOI: 10.1055/s-0042-101021 See also: Usefulness of training using animal models for colorectal endoscopic submucosal dissection: is experience performing gastric ESD really needed?Endosc Int Open 2016; 04(03): E333-E339DOI: 10.1055/s-0042-101022 See also: Refractory strictures despite steroid injection after esophageal endoscopic resectionEndosc Int Open 2016; 04(03): E354-E359DOI: 10.1055/s-0042-100903
Highlights from Recent Cancer Literature
Journal: Cancer Research (2015)

Posttranslational Modification Regulates Stem CellsIn breast cancer, aldehyde dehydrogenase (ALDH) activity is associated with highly aggressive tumors and poor outcome.To determine factors regulating ALDH1A1 activity Zhao and colleagues analyzed 10 putative lysine acetylation sites, identifying K353R and K353Q as regulating ALDH1A1 acetylation.Increased acetylation resulted in decreased ALDH1A1 enzyme activity, demonstrated by inhibitors of the sirtuin (SIRT) family of deacetylases (nicotinamide) and generation of highly acetylated recombinant ALDH1A1.In breast cancer stem cells NOTCH signaling promotes selfrenewal.Altered NOTCH signaling resulted in changes in SIRT2 protein levels, K353 acetylation, and ALDH1A1 enzyme activity.NOTCH signaling promotes breast cancer tumors in many ways.These studies suggest that Notch-driven induction of SIRT2 and posttranslational modification of ALDH1A1 stimulate enzyme activity and promote self-renewal.(Image by Emw courtesy of
Editorial board and contents
Authors: Andrew Sugden, Andrew Read, James Clark, Ian Owens, Paul Brakefield, Ragan Callaway, John Maron, Alan Gelfand, Peter Hudson, Andrew Dobson, Kevin Lafferty, Paul Moorcroft, Jason West, Gabriel Bowen, Thure Cerling, James Trendsin, Katrina Lythgoe, Linsey Meredith, Jon Fuller, Manager Moulton
Journal: Trends in Ecology & Evolution (2006)
Reducing Alcohol Use for Cancer Prevention
Authors: Neal D. Freedman, Christian C. Abnet
Journal: JAMA Network Open (2022)

Jung Eun Yoo, MD, PhD; Kyungdo Han, PhD; Dong Wook Shin, MD, MBA, DrPH; Dahye Kim, BS; Bong-seong Kim, MS; Sohyun Chun, MD; Keun Hye Jeon, MD; Wonyoung Jung, MD; Jinsung Park, MD, PhD; Jin Ho Park, MD, PhD; Kui Son Choi, PhD; Joo Sung Kim, MD, PhD
Assessment of Oncologists’ Perspectives on Omission of Sentinel Lymph Node Biopsy in Women 70 Years and Older With Early-Stage Hormone Receptor–Positive Breast Cancer
Authors: Christina A. Minami, Ava F. Bryan, Rachel A. Freedman, Anna C. Revette, Mara A. Schonberg, Tari A. King, Elizabeth A. Mittendorf
Journal: JAMA Network Open (2022)

Randomized clinical trial data have demonstrated that omission of surgical axillary evaluation does not affect overall survival in women 70 years and older with early-stage (clinical tumor category 1 [cT1] with node-negative [N0] disease) hormone receptor (HR)-positive and erb-B2 receptor tyrosine kinase 2 (ERBB2; formerly HER2)-negative breast cancer. Therefore, the Choosing Wisely initiative has recommended against routine use of sentinel lymph node biopsy (SLNB) in this population; however, retrospective data have revealed that more than 80% of patients eligible for SLNB omission still undergo the procedure. Multidisciplinary factors involved in these patterns remain unclear.To describe surgical, medical, and radiation oncologists' perspectives on omission of SLNB in women 70 years and older with cT1N0 HR-positive, ERBB2-negative breast cancer.This qualitative study used in-depth semi-structured interviews to explore the factors involved in oncologists' perspectives on providing care to older women who were eligible for SLNB omission. Purposive snowball sampling was used to recruit a sample of surgical, medical, and radiation oncologists representing a wide range of practice types and number of years in practice in the US and Canada. A total of 29 oncologists who finished training and were actively treating patients with breast cancer were interviewed. Interviews were conducted between March 1, 2020, and January 17, 2021.Recordings from semi-structured interviews were transcribed and deidentified. Thematic analysis was used to identify emergent themes.Among 29 physicians (16 women [55.2%] and 13 men [44.8%]) who participated in interviews, 16 were surgical oncologists, 6 were medical oncologists, and 7 were radiation oncologists. Data on race and ethnicity were not collected. Participants had a range of experience (median [range] years in practice, 12.0 [0.5-30.0]) and practice types (14 academic [48.3%], 7 community [24.1%], and 8 hybrid [27.6%]). Interviews revealed that the decision to omit SLNB was based on nuanced patient- and disease-level factors. Wide variation was observed in oncologists' perspectives on SLNB omission recommendations and supporting data. In addition, participants' statements suggested that the multidisciplinary nature of cancer care may increase oncologists' anxiety regarding SLNB omission.In this study, findings from interviews revealed that oncologists' perspectives may have implications for the largely unsuccessful deimplementation of SLNB in women 70 years and older with cT1N0 HR-positive, ERBB2-negative breast cancer. Interventions aimed at educating physicians, improving patient-physician communication, and facilitating preoperative multidisciplinary conversations may help to successfully decrease SLNB rates in this patient population.
Functional Connectivity of the Nucleus Accumbens and Changes in Appetite in Patients With Depression
Authors: Nils B. Kroemer, Nils Opel, Vanessa Teckentrup, Meng Li, Dominik Grotegerd, Susanne Meinert, Hannah Lemke, Tilo Kircher, Igor Nenadić, Axel Krug, Andreas Jansen, Jens Sommer, Olaf Steinsträter, Dana M. Small, Udo Dannlowski, Martin Walter
Journal: JAMA Psychiatry (2022)

Major depressive disorder (MDD) is characterized by a substantial burden on health, including changes in appetite and body weight. Heterogeneity of depressive symptoms has hampered the identification of biomarkers that robustly generalize to most patients, thus calling for symptom-based mapping.To define the functional architecture of the reward circuit subserving increases vs decreases in appetite and body weight in patients with MDD by specifying their contributions and influence on disease biomarkers using resting-state functional connectivity (FC).In this case-control study, functional magnetic resonance imaging (fMRI) data were taken from the Marburg-Münster FOR 2107 Affective Disorder Cohort Study (MACS), collected between September 2014 and November 2016. Cross-sectional data of patients with MDD (n = 407) and healthy control participants (n = 400) were analyzed from March 2018 to June 2022.Changes in appetite during the depressive episode and their association with FC were examined using fMRI. By taking the nucleus accumbens (NAcc) as seed of the reward circuit, associations with opposing changes in appetite were mapped, and a sparse symptom-specific elastic-net model was built with 10-fold cross-validation.Among 407 patients with MDD, 249 (61.2%) were women, and the mean (SD) age was 36.79 (13.4) years. Reduced NAcc-based FC to the ventromedial prefrontal cortex (vmPFC) and the hippocampus was associated with reduced appetite (vmPFC: bootstrap r = 0.13; 95% CI, 0.02-0.23; hippocampus: bootstrap r = 0.15; 95% CI, 0.05-0.26). In contrast, reduced NAcc-based FC to the insular ingestive cortex was associated with increased appetite (bootstrap r = -0.14; 95% CI, -0.24 to -0.04). Critically, the cross-validated elastic-net model reflected changes in appetite based on NAcc FC and explained variance increased with increasing symptom severity (all patients: bootstrap r = 0.24; 95% CI, 0.16-0.31; patients with Beck Depression Inventory score of 28 or greater: bootstrap r = 0.42; 95% CI, 0.25-0.58). In contrast, NAcc FC did not classify diagnosis (MDD vs healthy control).In this study, NAcc-based FC reflected important individual differences in appetite and body weight in patients with depression that can be leveraged for personalized prediction. However, classification of diagnosis using NAcc-based FC did not exceed chance levels. Such symptom-specific associations emphasize the need to map biomarkers onto more confined facets of psychopathology to improve the classification and treatment of MDD.
Study: New Wastewater Surveillance Method Detected SARS-CoV-2 Variants of Concern Up to 2 Weeks Before Clinical Tests
Authors: Jocelyn Solis-Moreira
Journal: JAMA (2022)

esearchers used a recently developed method of wastewater genomic surveillance to detect SARS-CoV-2 infections on the University of California, San Diego (UCSD), campus during 10 months of the pandemic.The approach identified viral variants of concern as early as 2 weeks before the variants showed up in clinical tests, the team recently reported in Nature.
Hyperbaric oxygen facilitates teniposide-induced cGAS-STING activation to enhance the antitumor efficacy of PD-1 antibody in HCC
Authors: Kun Li, Yihang Gong, Dongbo Qiu, Hui Tang, Jian Zhang, Zenan Yuan, Yingqi Huang, Yunfei Qin, Linsen Ye, Yang Yang
Journal: Journal for ImmunoTherapy of Cancer (2022)

Background Emerging evidence indicates that the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) axis plays a pivotal role in intrinsic antitumor immunity. Previous studies demonstrate that the conventional chemotherapy agent, teniposide, effectively promotes the therapeutic efficacy of programmed cell death protein-1 antibody (PD-1 Ab) through robust cGAS-STING activation. Unfortunately, the cGAS expression of tumor cells is reported to be severely suppressed by the hypoxic status in solid tumor. Clinically, enhancing chemotherapy-induced, DNA-activated tumor STING signaling by alleviating tumor hypoxia might be one possible direction for improving the currently poor response rates of patients with hepatocellular carcinoma (HCC) to PD-1 Ab. Methods Teniposide was first screened out from several chemotherapy drugs according to their potency in inducing cGAS-STING signaling in human HCC cells. Teniposide-treated HCC cells were then cultured under hypoxia, normoxia or reoxygenation condition to detect change in cGAS-STING signaling. Next, oxaliplatin/teniposide chemotherapy alone or combined with hyperbaric oxygen (HBO) therapy was administered on liver orthotopic mouse tumor models, after which the tumor microenvironment (TME) was surveyed. Lastly, teniposide alone or combined with HBO was performed on multiple mouse tumor models and the subsequent anti-PD-1 therapeutic responses were observed. Results Compared with the first-line oxaliplatin chemotherapy, teniposide chemotherapy induced stronger cGAS-STING signaling in human HCC cells. Teniposide-induced cGAS-STING activation was significantly inhibited by hypoxia inducible factor 1α in an oxygen-deficient environment in vitro and the inhibition was rapidly removed via effective reoxygenation. HBO remarkably enhanced the cGAS-STING-dependent tumor type Ⅰ interferon and nuclear factor kappa-B signaling induced by teniposide in vivo, both of which contributed to the activation of dendritic cells and subsequent cytotoxic T cells. Combined HBO with teniposide chemotherapy improved the therapeutic effect of PD-1 Ab in multiple tumor models. Conclusions By combination of two therapies approved by the Food and Drug Administration, we safely stimulated an immunogenic, T cell-inflamed HCC TME, leading to further sensitization of tumors to anti-PD-1 immunotherapy. These findings might enrich therapeutic strategies for advanced HCC andwe can attempt to improve the response rates of patients with HCC to PD-1 Ab by enhancing DNA-activated STING signaling through effective tumor reoxygenation.
Microglial TYROBP/DAP12 in Alzheimer’s disease: Transduction of physiological and pathological signals across TREM2
Authors: Jean-Vianney Haure-Mirande, Mickael Audrain, Michelle E. Ehrlich, Sam Gandy
Journal: Molecular Neurodegeneration (2022)

Abstract TYROBP (also known as DAP12 or KARAP) is a transmembrane adaptor protein initially described as a receptor-activating subunit component of natural killer (NK) cells. TYROBP is expressed in numerous cell types, including peripheral blood monocytes, macrophages, dendritic cells, and osteoclasts, but a key point of recent interest is related to the critical role played by TYROBP in the function of many receptors expressed on the plasma membrane of microglia. TYROBP is the downstream adaptor and putative signaling partner for several receptors implicated in Alzheimer’s disease (AD), including SIRP1β, CD33, CR3, and TREM2. TYROBP has received much of its current notoriety because of its importance in brain homeostasis by signal transduction across those receptors. In this review, we provide an overview of evidence indicating that the biology of TYROBP extends beyond its interaction with these four ligand-binding ectodomain-intramembranous domain molecules. In addition to reviewing the structure and localization of TYROBP, we discuss our recent progress using mouse models of either cerebral amyloidosis or tauopathy that were engineered to be TYROBP-deficient or TYROBP-overexpressing. Remarkably, constitutively TYROBP-deficient mice provided a model of genetic resilience to either of the defining proteinopathies of AD. Learning behavior and synaptic electrophysiological function were preserved at normal physiological levels even in the face of robust cerebral amyloidosis (in APP/PSEN1 ; Tyrobp −/− mice) or tauopathy (in MAPT P301S ; Tyrobp −/− mice). A fundamental underpinning of the functional synaptic dysfunction associated with each proteotype was an accumulation of complement C1q. TYROBP deficiency prevented C1q accumulation associated with either proteinopathy. Based on these data, we speculate that TYROBP plays a key role in the microglial sensome and the emergence of the disease-associated microglia (DAM) phenotype. TYROBP may also play a key role in the loss of markers of synaptic integrity (e.g., synaptophysin-like immunoreactivity) that has long been held to be the feature of human AD molecular neuropathology that most closely correlates with concurrent clinical cognitive function.
Glutathione peroxidase 2 is a metabolic driver of the tumor immune microenvironment and immune checkpoint inhibitor response
Authors: Kazi Mokim Ahmed, Ratna Veeramachaneni, Defeng Deng, Nagireddy Putluri, Vasanta Putluri, Maria F Cardenas, David A Wheeler, William K Decker, Andy I Frederick, Sawad Kazi, Andrew G Sikora, Vlad C Sandulache, Mitchell J Frederick
Journal: Journal for ImmunoTherapy of Cancer (2022)

Background The existence of immunologically ‘cold tumors’ frequently found across a wide spectrum of tumor types represents a significant challenge for cancer immunotherapy. Cold tumors have poor baseline pan-leukocyte infiltration, including a low prevalence of cytotoxic lymphocytes, and not surprisingly respond unfavorably to immune checkpoint (IC) inhibitors. We hypothesized that cold tumors harbor a mechanism of immune escape upstream and independent of ICs that may be driven by tumor biology rather than differences in mutational neoantigen burden. Methods Using a bioinformatic approach to analyze TCGA (The Cancer Genome Atlas) RNA sequencing data we identified genes upregulated in cold versus hot tumors across four different smoking-related cancers, including squamous carcinomas from the oral cavity (OCSCC) and lung (LUSC), and adenocarcinomas of the bladder (BLCA) and lung (LUAD). Biological significance of the gene most robustly associated with a cold tumor phenotype across all four tumor types, glutathione peroxidase 2 (GPX2), was further evaluated using a combination of in silico analyses and functional genomic experiments performed both in vitro and in in vivo with preclinical models of oral cancer. Results Elevated RNA expression of five metabolic enzymes including GPX2, aldo-keto reductase family 1 members AKR1C1, AKR1C3, and cytochrome monoxygenases (CP4F11 and CYP4F3) co-occurred in cold tumors across all four smoking-related cancers. These genes have all been linked to negative regulation of arachidonic acid metabolism—a well-established inflammatory pathway—and are also known downstream targets of the redox sensitive Nrf2 transcription factor pathway. In OCSCC, LUSC, and LUAD, GPX2 expression was highly correlated with Nrf2 activation signatures, also elevated in cold tumors. In BLCA, however, GPX2 correlated more strongly than Nrf2 signatures with decreased infiltration of multiple leukocyte subtypes. GPX2 inversely correlated with expression of multiple pro- inflammatory cytokines/chemokines and NF-kB activation in cell lines and knockdown of GPX2 led to increased secretion of prostaglandin E2 (PGE2) and interleukin-6. Conversely, GPX2 overexpression led to reduced PGE2 production in a murine OCSCC model (MOC1). GPX2 overexpressing MOC1 tumors had a more suppressive tumor immune microenvironment and responded less favorably to anti-cytotoxic T-lymphocytes-associated protein 4 IC therapy in mice. Conclusion GPX2 overexpression represents a novel potentially targetable effector of immune escape in cold tumors.